Lung surfactant production is being studied by assessment of its principal phospholipid component, phosphatidylcholine (PC). The primary mechanism for lung PC synthesis in the fetus has been identified as the choline pathway. Tissue cultured lung cells have been studied and found to show marked enrichment in choline pathway enzymes and greater rates of phospholipid synthesis than any source studied to date. Lung PC concentration has been shown to increase during the latter 10-20 percent of gestation in many fetal species. Increased choline pathway enzyme activities accompany this change and may be induced by injection of animals with either cortisol or thyroxin. Pressure-volume hysteresis, deflation stability, and the content of surface active material have been evaluated in lungs from developing monkey fetuses and found to change in accordance with the biochemical events of maturation. In addition to promoting lung differentiation, administration of corticosteroids to pregnant monkeys has been found to accelerate the development of other organs including liver and kidney. Marked increases in hepatic glycogen levels were demonstrated within 48 hours after maternal administration of a cortisol analog. Thus, corticosteroids may provide the stimulus for maturation of many fetal organs. Promising data from clinical trials elsewhere suggest that these agents may be useful in the prevention of the respiratory distress syndrome of human neonates.